Expression Of VEGF,TGF-β1and GM-CSF In Nasal Polyps And Nasal Polyposis | | Posted on:2013-02-24 | Degree:Master | Type:Thesis | | Country:China | Candidate:Y Liu | Full Text:PDF | | GTID:2214330374459022 | Subject:Otorhinolaryngology | | Abstract/Summary: | PDF Full Text Request | | Objective: Nasal polyps and nasal polyposis are upper airway chronicinflammatory diseases. The pathogeneses leading to these diseases areindefinite. Nasal polyps and nasal polyposis are characterized with epitheliumhyperplasia and squamous metaplasia, extracellular matrix accumulation andfibrosis, interstitial edema and vascular proliferation, a lot of inflammatorycells infiltration in histopathology. There are complicated pathology processesalong with their genesis and development. Many kinds of cytokines continueexistence in their morbidity. Vascular endothelial growth factor(VEGF) caneffect specially vascular endothelial cell. It stimulates vascular endothelial celldivision growth and at last leads to neovascularization. It also has the role ofincreasing vasopermeability. Transforming growth factor-β1(TGF-β1)possesses general biologic activities. The distinguished function is to promotethe production of extracellular matrix among them. Granulocyte-macrophagecolony-stimulation factor(GM-CSF) has many contributions to monocyticseries and granulocytic series, such as maintaining survivals, inducing andadvancing colony growth, causing their function strengthen. To study theexpression of vascular endothelial growth factor (VEGF), transforminggrowth factor-β1(TGF-β1) and granulocyte-macrophage colony-stimulationfactor(GM-CSF) in nasal polyposis, nasal polyps and inferior turbinatemucosa tissues and investigate the probable functions of them in nasalpolyposis and nasal polyps pathogeneses.Methods: grouping, choosing cases, obtaining specimens. Dividing intothree groups: nasal polyps, nasal polyposis and inferior turbinate mucosa(control) group. All of the specimens were from December2009~March2011in need of endoscopic sinus surgery in our hospital.28nasal polypstissues were come from the patients(males18, females10: age range18~55 years, mean age36.4years).21nasal polyposis tissues were obtained fromthe patients(males14,females7:age range21~68years, mean age46years).16inferior turbinate mucosa tissues as control group were from thepatients(males11,females5:age range22~45years, mean age34years) ofseptal deviation with hypertrophic inferior turbinate. All cases had not thepatient history of general disease, immune system disease and other nasaldisease. All patients stopped using general and topic remedy before one month.The samples were fixed into4%paraform, been routine dehydration,embedded into paraffine. Tissue slices were counted with HE staining methodfor eosinophile granulocyte in each group tissue. The expression of VEGF,TGF-β1and GM-CSF was observed by means of immunohistochemistry innasal polyps, nasal polyposis and control groups. To confer the difference ofpositive rate of VEGF,TGF-β1,GM-CSF in three groups. To compare thevariance of positive cell count of VEGF,TGF-β1,GM-CSF in nasal polyposisand nasal polyps groups. The gained data were applied by SPSS13.0toaccording statistical analysis.Result:1The detection rates of VEGF were76.2%and57.1%in nasal polyposis andnasal polyps tissues respectively. The detection rate of VEGF was12.5%ininferior turbinate mucosa tissues. They were significantly higher than ininferior turbinate mucosa tissues (P<0.0167). But the detection rate ofVEGF was not different in nasal polyposis and nasal polypstissues(P=0.166>0.0167). VEGF was located mainly in the inflammatorycells under the basilar membrane and endothelial and vicinal cells aroundthe vessel in nasal polyposis and nasal polyps tissues. The positive cellcount of VEGF in the inflammatory cells under the basilar membrane andendothelial and vicinal cells around the vessel was significantly higher innasal polyposis than in nasal polyps tissues(P<0.01and P<0.01).2The detection rates of TGF-β1were100%and64.3%in nasal polyposis andnasal polyps tissues respectively. The detection rate of TGF-β1was12.5%in inferior turbinate mucosa tissues. They were significantly higher than in inferior turbinate mucosa tissues and significantly different in comparisonwith each other(P<0.0167). The TGF-β1of nasal polyposis and nasalpolyps tissues was not only to present chiefly in the superficialis laminapropria, but also in extracellular matrix. The positive cell count of TGF-β1in the lamina propria in nasal polyposis tissues was significantly higher thanin nasal polyps tissues(P<0.01). The distribution of TGF-β1expressingcells in nasal polyposis and nasal polyp tissues was similar to those ofeosinophils, their expressions were positive correlation (r1=0.683,P<0.01,r2=0.772, P<0.01). Quantities of eosinophils that were TGF-β1positivity inthe two groups had also obvious variance by contrasting(P<0.01).3The detection rates of GM-CSF were71.4%and35.7%in nasal polyposisand nasal polyps tissues respectively. The detection rate of GM-CSF was0%in inferior turbinate mucosa tissues. They were significantly higher thanin inferior turbinate mucosa tissues and significantly different incomparison with each other.(P<0.0167). The positive cell of GM-CSFexpressed mainly under the mucosa and around the blood vessel and wasprincipally eosinophils. The positive cell count of GM-CSF in the stroma innasal polyposis tissues was significantly higher than in nasal polypstissues(P<0.01). There was positive correlation between the positive cellcount of GM-CSF and the number of eosinophils that were GM-CSFpositivity in nasal polyposis and nasal polyps tissues (r1=0.651, P<0.01,r2=0.684, P<0.01). Quantities of eosinophils that were GM-CSF positivityin the two groups had also obvious variance by contrasting(P<0.01).4Nasal polyps and nasal polyposis tissures were coveraged bypseudostratified ciliated columnar epithelium and seen squamous metaplasiapartly, their epithelium were thicken and glandular organ are hyperplasied,there were loose connective tissues in stroma with blood vessel expansionand there were distinct quantities of inflammatory cells in nasal polyps andnasal polyposis tissures by the HE staining method. The infiltrative cellcount of eosinophils in nasal polyposis, nasal polyps and inferior turbinatemucosa tissues had significantly difference in comparison with each other(P<0.01).Conclusion:1Nasal polyposis and nasal polyps are main characterized by eosinophilsaccumulation which are chronic imflammation diseases.2VEGF plays a key role in the progression of tissue edema and vascularproliferation in nasal polyps and nasal polyposis. The overexpression ofVEGF in nasal polyps may contribute to the growth of vessles,accumulation of inflammatory cells, organism heavy edema, as a result, toenhance the morbidity of nasal polyposis.3TGF-β1may contribute to some of the pathologic changes observed in nasalpolyps and nasal polyposis, such as extracellular matrix fibrosis andthickening of the epithelial basement membrane.4GM-CSF is the main cytokine that sustains the eosinophils survival. It mayrestrain eosinophils apoptosis and make eosinophils survival timeincreasing. It also has chemotaxis and activation to eosinophils. Theseinduce GM-CSF to diffuse and concentrate generously towards thesurrounding mucosa. Then these lead to the part inflammation existencepersistently and repeatedly. Pathological changes involve many groups ofnasal sinuses. Those changes promote endlessly development of nasalpolyps and nasal polyposis.5TGF-β1and GM-CSF in nasal polyps and nasal polyposis tissures may comefrom Eosinophils mainly. | | Keywords/Search Tags: | nasal polyps, nasal polyposis, vascular endothelial growthfactor, transforming growth factor-β1, granulocyte-macrophage colony-stimulation factor | PDF Full Text Request | Related items |
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